ObjectiveTo investigate relationship between ultrastructural changes and expression of basic fibroblast growth factor of diabetic retinopathy in rats.MethodsDiabetes was induced in rats with a single injection of streptozotocin (STZ) and divided into normal control group and 1- , 3- and 5- month diabetes group. The paraffin slide was observed by in-situ hybridization and immunohistochemistry, and retinal ultrastructure was examined by transmission electron microscopy.ResultsNo change of retinal ultrastructure was found in the control group. Different degrees of ultrastructure lesion were found in 1-month diabetic rats with fragmental increase of thickness of basement membrane, swelling of endothelial cells and obvions fingerlike processes in the capillary cavity, disconcentration of heterochromatin both in endothelium and pericyte, and swelling and degeneration of mitochondrion. The edema of endothelial cells of 3-month diabetic rats was more serious than that of 1month ones, and the capillary cavity was nearly occluded. In 5-month diabetic rats, the basement membrane was unevenly thickened, or obviously split. The positive rate of in-situ hybridization in 3-month diabetic rats was 77.8% while the positive rate of immunohistochemical stain was 55.6%, which increased to 88.9% in 5-month diabetic rats.ConclusionsThe occurrence of the ultrastructural changes in STZ rats with diabetic retinopathy is earlier than that of the expression of bFGF.(Chin J Ocul Fundus Dis, 2003,19:348-351)
Retinal diseases are severely limited in terms of effective treatment strategies due to their extremely complex pathogenesis. Given the limitations of traditional mammalian experimental animals in replicating certain characteristics of eye diseases, the zebrafish model, with its advantages such as fully transparent embryos facilitating in vivo tracking, extremely early development of visual functions, highly conserved retinal cell composition compared to humans, and the ability to regenerate neurons completely after damage, has risen to become a core tool for visual system research. Through modern technologies such as gene editing, RNA knockdown, and chemical induction, researchers have successfully constructed a zebrafish model system that highly mimics various genetic and non-genetic retinal disorders in humans. In non-genetic disorders, this model effectively replicates microvascular abnormal proliferation and electrophysiological changes caused by high sugar or low oxygen stress, and has been successfully applied to the efficacy evaluation of natural products and nanodelivery systems. In the exploration of genetic disorders, for complex diseases such as photoreceptor degeneration, nutritional disorders of cone and rod cells, early severe vision loss, defect in signal transduction-induced night blindness, and multi-system ciliary abnormalities syndrome, the zebrafish model precisely reproduces the corresponding clinical phenotypes. More importantly, it plays a decisive role in elucidating the functions of new pathogenic genes, clarifying the disorder of the light conduction pathway, revealing the multi-gene collaborative pathogenic network, and discovering new candidate pathogenic sites. Additionally, in the in vivo safety testing of nonsense mutation read-through drugs and functional rescue verification, the zebrafish model also demonstrates high clinical translational potential. The zebrafish model, by closely linking genetic variations with in vivo pathological phenotypes, has overcome the limitations of in vitro research. It not only provides an ideal platform for in-depth analysis of the pathogenesis of blinding diseases, exploration of molecular switches for neural regeneration, and provides a solid foundation for accelerating high-throughput screening of targeted drugs and promoting individualized precision medicine, but also has extremely broad application prospects in the future.